Fibrosis has been considered as a hallmark of dysfunctional adipose tissue (AT), however the role and mechanisms of fibrosis in the age related AT dysfunction are not yet well characterized.

The aim of the study was to investigate the mechanisms of extracellular matrix (ECM) alterations and the role of caveolins, using an in vitro model of adipocyte aging and hypoxia.

Hypoxic adipocytes, but also aged adipocytes, were characterized by a significant increase in gene expression of pro-inflammatory cytokines and ECM components. Immunofluorescence analysis confirmed an increase in collagen VI-A3 in hypoxic and also in aged adipocytes. However aged adipocytes were characterized by only a slight increase in HIF1α immunofluorescence and by a more relevant increase in senescence compared to hypoxic and mature adipocytes, with an increase in p-53 protein and a decrease in SIRT 1 protein.

Immunofluorescence and western blot analysis revealed a significant decrease in caveolin-1 expression in hypoxic adipocytes and even more in aged adipocytes.

In conclusions, aging adipocytes are associated to alteration of ECM and fibrosis, by modulation of the caveolins through complex mechanisms where inflammation, hypoxia and cellular senescence are coexisting.

纤维化被认为是功能失调的脂肪组织 (AT) 的标志，但是纤维化在与年龄相关的 AT 功能障碍中的作用和机制尚未得到很好的表征。

该研究的目的是使用脂肪细胞老化和缺氧的体外模型研究细胞外基质 (ECM) 改变的机制和小窝蛋白的作用。

缺氧脂肪细胞以及老化脂肪细胞的特征是促炎细胞因子和 ECM 成分的基因表达显着增加。免疫荧光分析证实了在缺氧和老化脂肪细胞中胶原蛋白 VI-A3 的增加。然而，与缺氧和成熟脂肪细胞相比，衰老脂肪细胞的特征是 HIF1α 免疫荧光仅略有增加，衰老的增加更相关，p-53 蛋白增加，SIRT 1 蛋白减少。

免疫荧光和蛋白质印迹分析显示缺氧脂肪细胞中caveolin-1 表达显着降低，在老化脂肪细胞中的表达甚至更多。

总之，通过炎症、缺氧和细胞衰老共存的复杂机制调节小窝蛋白，衰老脂肪细胞与 ECM 的改变和纤维化有关。